Surgical techniques have been developed in recent years for the replacement of damaged or diseased joints, amputations, resections for malignancy or disease, and various types of malformation. Complete or partial replacement of the coxo-femoral or hip joint is one of the most common operations in this area, particularly among the elderly or in patients having severe arthritic conditions. Initially, hip joint surgery was limited to the repair or replacement of the femoral head, which in many of the earlier procedures was accomplished by an autologous bone graft. The major limitation of such a procedure is the necessity for opening a second surgical site to remove healthy bone for replacement into the damaged skeletal member. Moreover, the surgeon must form the healthy bone in the desired configuration in an autologous bone graft procedure within the limited time period of the operation.
Improved prosthetic devices have been developed and are now used as attachments, reinforcements or replacements to hip joints and various other skeletal members as an alternative to bone graft procedures. The primary considerations in the design of any prosthetic device is to effectively simulate the operation of a damaged body member over an extended period of time, and to achieve compatibility with the body in the damaged area. In load carrying skeletal members subjected to high stresses, such as the hip joint, compatability is achieved by not only avoiding rejection or toxic reaction of the body to the materials used in the prosthesis, but also by allowing the adjacent bone to have stresses and carry loads as if the natural hip joint was not removed.
The starting point in the design of a biocompatible coxo-femoral joint prosthesis at a recognition of the dynamics of bone growth and adaptation, and the highly controlled cellular behavior responsible for the form, size and location of bone. The cellular content of bone includes mesenchymal cells which are normally distributed on the bone surface and in miscroscopic spaces of bones. In response to loading of the bone, the mesenchymal cells become "activated" and undergo division to produce osteoclasts, or bone destroying cells. The osteoclasts undergo an internal nuclear transformation after some period has elapsed in the metabolic sequence to form osteoblasts, which are bone producing cells. Under ideal conditions, as bones in the healthy individual are subjected to normal loads and stresses, the bone destroyed by the osteoclasts equals that produced by the osteoblasts. In the event of a disruption of normal stress concentration and loading in a bone, such as what would result after a fracture, the mesenchymal cells are activated and extracellular agencies operate to selectively inhibit the activity of the osteoclasts, allowing the osteoblastic activity to dominate and replace the bone in the fractured area.
Many of the prior art hip joint prosthesis include rigid metal components having a modulus of elasticity or bending stiffness much greater than that of the femur or the acetabulum of the pelvis. Clinical studies have confirmed that such prior art prostheses often loosen after a period of years or months due to bone resorption and necrotic degeneration of the affected area, requiring a second operation in many instances. It is believed that such resorption and necrotic degeneration are caused by at least two factors. First, the localized pressure imposed on the adjacent bone by the rigid metal components tends to pinch off blood vessels and crush adjacent tissue. In addition, the relatively high resistance to bending of the rigid metal components compared to the bone in the medullary canal of the femur and in the acetabulum, creates unnatural stress concentrations in the adjacent bone. Rather than providing for natural distribution of loads and stresses on the femur and acetabulum, such prior art prostheses carry the major portion of the load imposed on the coxo-fermoral joint and adjacent bone. What the body senses is a reduction of the normal stress carrying demand on the femur and acetabulum. The mesenchymal cells are activated, but instead of the normal activity of osteoclasts and osteoblasts in a healthy bone, extracellular agencies operate to inhibit osteoblastic activity resulting in overall resorption of the bone by the osteoclasts. Thus the femur and acetabulum undergo resorption resulting in a loosening of the prosthesis after a period of time. Unfortunately, such resorption and the necrotic degeneration produced by uneven stress concentration and localized pressure may not be detected until the patient is partially rehabilitated and has begun attempts to utilize the affected skeletal member in normal activity.
The problem of localized pressure and uneven stress distribution has at least been recognized in some of the prior art patents, but a hip joint prosthesis capable of overcoming such problems was not available prior to development of the subject invention. U.S. Pat. No. 3,707,006 to Bokros et al, for example, discloses a porous ceramic substrate impregnated with a resin to obtain a joint prosthesis intended to flex and bend with the bone to avoid stress concentration at the metal-bone interface as experienced in prior art rigid metal prostheses. It is doubtful that the brittle ceramic substrate can provide a bending stiffness approximating that of bone over an extended period, and it has been found to be difficult to obtain bone and tissue ingrowth into the surface of the Bokros et al prosthesis without some type of surface treatment which tends to weaken the entire structure.
Another approach is found in U.S. Pat. No. 3,938,198 to Kahn et al, which discloses a hip joint prosthesis having a rigid solid stem covered with a layer or jacket of resilient elastomer to cushion applied loads and stresses. While some of the shock imposed on the hip and femur may be absorbed and distributed by the elastomeric layer, the Kahn et al devices does nothing to alter the bending stiffness of the stem portion which will be governed by the stiffness of the rigid metal component. In addition, the elastomer jacket of Kahn et al is covered with a fibrous overlayer formed of Dacron (polyethylene terephthalate) woven mesh, to enhance bone ingrowth. Other fibrous attachments commonly in use include polysulfone and Proplast which is a Teflon.sup.R coated graphite fiber mat. As is well known, a surface porosity of about 100 microns is needed to promote bone ingrowth, while primarily tissue ingrowth will occur with less than a 100 micron surface porosity. Recent clinical studies have shown that such low modulus fibrous attachments as mentioned above promote tissue ingrowth but not bone ingrowth, regardless of the original pore size of the material used. It is believed that the absence of bone ingrowth may be attributed to local movement of the fibrous attachments and a reduction of their pore size resulting from applied loads.
Another problem associated with existing hip joint prostheses is their inability to remain in position during the crucial rehabilitation phase where bone ingrowth takes place. This is not a concern in prostheses embedded in position with bone cement, but it has been found that problems with this technique include incomplete filing of the cavity of the bone, toxicity of the cement and possible necrosis of the adjacent layer of bone. In addition, it has been found that a prosthesis held in place by good bone ingrowth exhibits better stability and may result in better stress distribution to adjacent bone than those embedded in bone cement.
Those prior art hip joint prostheses which utilize a porous outerlayer to enhance bone ingrowth, are typically held in place by pins attached to the femur and pelvis adjacent the interface between the femur and acetabulum. The Kahn et al patent is one example. Although the problem of prosthesis stability during the early stages of bone ingrowth may not be serious in skeletal members which can easily be placed in a cast or otherwise restricted from movement, it is very difficult to avoid movement of the hip joint unless the patient is totally immobilized. Some movement of the affected hip is virtually unavoidable. Merely pinning the hip prosthesis at the femur-actebulum interface does not prevent movement of the stem portion of the prosthesis within the femoral medullary canal. Moreover, the location and implantation of such pins adds another step to the operating procedure which can be avoided as discussed below.